ObjectiveTo investigate the migration and distribution characteristics of chemical constituents in blood and hippocampal tissues before and after vinegar processing of Citri Reticulatae Pericarpium Viride（CRPV）， and to explore the potential material basis and mechanisms underlying their regulatory effects on emotional disorders by comparing the effects of raw and vinegar-processed products of CRPV. MethodsUltra-performance liquid chromatography-quadrupole-time-of-flight mass spectrometry（UPLC-Q-TOF-MS/MS） was employed to characterize and identify the chemical constituents of raw and vinegar-processed products of CRPV extracts， as well as their migrating components in blood and hippocampal tissues after oral administration. Reference standards， databases， and relevant literature were utilized for compound annotation， with data processing performed using PeakView 1.2 software. Seventy male C57BL/6 mice were randomly divided into seven groups， including the blank group， model group， diazepam group（2.5 mg·kg^-1）， raw CRPV low/high dose groups（0.6， 1.2 g·kg^-1）， and vinegar-processed CRPV low/high dose groups（0.6， 1.2 g·kg^-1）， with 10 mice per group. Except for the blank group， all other groups underwent chronic restraint stress（2 h·d^-1） for 20 d. Each drug-treated group received oral administration at the predetermined dose starting 10 d after modeling， with a total treatment duration of 10 d. Following model-based drug administration， mice underwent open-field， forced swimming， and elevated plus maze tests. After anesthesia with isoflurane， whole brains were collected from each group of mice， and hippocampi were dissected. Reactive oxygen species（ROS） level in hippocampal tissues was quantified by enzyme-linked immunosorbent assay（ELISA）. Hematoxylin-eosin（HE） staining was used to observe hippocampal tissue morphology. Immunofluorescence was performed to detect neuronal nuclei（NeuN） and peroxisome proliferator-activated receptor alpha（PPARα） expressions in hippocampal tissue. Then， pharmacodynamic evaluations were conducted to assess the effects of raw and vinegar-processed CRPV on mood disorders， exploring the potential mechanisms. ResultsVinegar processing caused significant changes in the chemical composition of CRPV， with 18 components showing increased relative content and 35 components showing decreased relative content. The primary changes occurred in flavonoid compounds， including 20 flavonoids， 20 flavonoid glycosides， 3 triterpenes， 3 phenolic acids， 1 alkaloid， and 6 other compounds. Twenty-one components were detected in blood（15 methoxyflavones， 4 flavonoid glycosides， and 2 phenolic acids）， with 17 shared between raw and vinegar-processed CRPV. Seven components reached hippocampal tissues（all common to both forms）. In regulating emotional disorders， Vinegar-processed CRPV exhibited superior antidepressant-like effects compared to raw products. HE staining revealed that both treatments improved hippocampal neuronal morphology， particularly in the damaged CA1 and CA3 regions. Immunofluorescence and ELISA analyses demonstrated that both raw and vinegar-processed CRPV significantly modulated NeuN and PPARα expressions in hippocampal tissue while alleviating oxidative stress induced by excessive ROS（P<0.05）. ConclusionThe chemical composition of CRPV undergoes changes after vinegar processing， but the migrating components in blood and hippocampus are primarily methoxyflavonoids. These components may serve as the potential material basis for activating the PPARα pathway， thereby negatively regulating ROS generation in the hippocampus， reducing oxidative stress， and promoting the development of NeuN-positive neurons. These findings provide experimental evidence for enhancing quality standards， pharmacodynamic material research， and active drug development of raw and vinegar-processed CRPV.

Chronic liver diseases are a group of diseases in which the liver is subjected to a variety of injuries over a long period of time， resulting in irreversible pathological changes that last longer than 6 months. Emodin （EMO） is a natural anthraquinone derivative derived from Rheum officinale， and its pharmacological effect has been extensively studied， exhibiting a variety of biological properties and involving multiple signaling molecules and pathways. Western medicine or surgical treatment is currently the main treatment regimen for chronic liver diseases， and the advance in treatment is limited by various reasons such as side effects and high costs. Due to its natural origin and efficacy， EMO has unique advantages in the treatment of chronic liver diseases and has now become a research hotspot. This article summarizes the therapeutic effect of EMO on chronic liver diseases and its mechanism， in order to provide a certain scientific basis for the traditional Chinese medicine treatment of chronic liver diseases and the development of drugs in clinical practice.

Background: This study was performed to characterize the incidence, costs, and risk factors associated with renal and cardiovascular adverse outcomes following primary percutaneous coronary intervention (pPCI) in patients with ST-elevation myocardial infarction (STEMI). Methods: Patients with STEMI who underwent pPCI using iso-osmolar contrast were enrolled at 39 centers. The incidence of acute kidney injury (AKI) and major adverse renal and cardiovascular events (MARCE) was analyzed, as well as inpatient costs. Logistic regression analysis was performed to identify risk factors. Results: Among 2,293 patients, the incidence of AKI and MARCE within 72 hours post-pPCI was 4.14% (n = 95) and 4.40% (n = 101), respectively. AKI and/or MARCE were associated with systolic blood pressure (AKI: odds ratio [OR], 1.009; 95% confidence interval [CI], 1.000–1.018), hypertension (AKI: OR, 1.815; 95% CI, 1.133–2.906; MARCE: OR, 1.760;95% CI, 1.118–2.769), anterior wall infarction (AKI: OR, 1.895; 95% CI, 1.196–3.004; MARCE:OR, 1.939; 95% CI, 1.240–3.032), Killip class (AKI: OR, 1.465; 95% CI, 1.117–1.922; MARCE:OR, 1.467; 95% CI, 1.131–1.903), and serum creatinine (SCr; MARCE: OR, 1.006; 95% CI, 1.000–1.012). Hospitalization costs for patients with STEMI who developed AKI or MARCE were significantly higher than for those without AKI (9,595 ± 5,795 vs. 8,279 ± 3,872 USD, P = 0.003) or without MARCE (9,890 ± 5,616 vs. 8,255 ± 3,859 USD, P < 0.001). Conclusions In patients with STEMI undergoing pPCI with iso-osmolar contrast, the incidence of AKI and MARCE was associated with higher hospitalization costs. Systolic blood pressure, hypertension, anterior wall infarction, Killip class, and SCr were identified as risk factors for these outcomes.

Objective To systematically evaluate the risk prediction models for anastomotic leakage (AL) in patients with esophageal cancer after surgery. Methods A computer-based search of PubMed, EMbase, Web of Science, Cochrane Library, Chinese Medical Journal Full-text Database, VIP, Wanfang, SinoMed and CNKI was conducted to collect studies on postoperative AL risk prediction model for esophageal cancer from their inception to October 1st, 2023. PROBAST tool was employed to evaluate the bias risk and applicability of the model, and Stata 15 software was utilized for meta-analysis. Results A total of 19 literatures were included covering 25 AL risk prediction models and 7373 patients. The area under the receiver operating characteristic curve (AUC) was 0.670-0.960. Among them, 23 prediction models had a good prediction performance (AUC>0.7); 13 models were tested for calibration of the model; 1 model was externally validated, and 10 models were internally validated. Meta-analysis showed that hypoproteinemia (OR=9.362), postoperative pulmonary complications (OR=7.427), poor incision healing (OR=5.330), anastomosis type (OR=2.965), preoperative history of thoracoabdominal surgery (OR=3.181), preoperative diabetes mellitus (OR=2.445), preoperative cardiovascular disease (OR=3.260), preoperative neoadjuvant therapy (OR=2.977), preoperative respiratory disease (OR=4.744), surgery method (OR=4.312), American Society of Anesthesiologists score (OR=2.424) were predictors for AL after esophageal cancer surgery. Conclusion At present, the prediction model of AL risk in patients with esophageal cancer after surgery is in the development stage, and the overall research quality needs to be improved.

Objective To investigate the effect of Pirfenidone(PFN)on respiratory syncytial virus(RSV)infection-induced damage to bronchial epithelial cells by regulating the high mobility group protein B1(HMGB1)/receptor for advanced glycation end products(RAGE)signaling pathway.Methods Human bronchial epithelial cells(HBE)were divided into Control group(cultured for 24 h under normal conditions),RSV group(inoculated with 4.65×106/mL RSV at 33℃for 2 h);low PFN(L-PFN)group(treated with 0.05 mg/mL PFN for 24 h),moderate PFN(M-PFN)group(treated with 0.10 mg/mL PFN for 24 h),high PFN(H-PFN)group(treated with 0.20 mg/mL PFN for 24 h)and recombinant HMGB1(rHMGB1)group(treated with 1 μg/mL rHMGB1+0.20 mg/mL PFN for 24 h).EdU method was applied to detect the proliferation rate of cells in each group,Hochest33258 staining method was applied to detect apoptosis status of cells in each group,and the migration of cells in each group was evaluated by the scratch experiment.Enzyme linked immunosorbent assay(ELISA)was applied to measure the levels of interferon(IFN)-α,IFN-γ,tumor necrosis factor-α(TNF-α),interleukin(IL)-1α,IL-6 and IL-4 in each group of cells,and Western blot was applied to detect the protein expression of HMGB1,RAGE,B lymphoblastoma-2-associated X protein(Bax),cysteine aspartic protease-3(Caspase-3),and B lymphoblastoma-2(Bcl-2).Results Compared with the RSV group,the cell proliferation rate,scratch closure rate,IL-4 levels,and expression of Bcl-2 in L-,M-,and H-PFN groups increased,while the apoptosis rate,the levels of IFN-α,IFN-γ,TNF-α,IL-1α,IL-6,and the expression of HMGB1,RAGE,Bax,and Caspase-3 reduced(P<0.05);rHMGB1 weakened the effect of H-PFN on the above-mentioned indicators(P<0.05).Conclusion PFN may suppress the apoptosis and inflammatory damage of RSV-infected bronchial epithelial cells by inhibiting the HMGB1/RAGE pathway.Conclusion PFN may suppress the apoptosis and inflammatory damage of RSV-infected bronchial epithelial cells by inhibiting the HMGB1/RAGE pathway.

The clinical diagnosis and treatment of urinary tract infection has long faced the challenges of insufficient standardization of diagnosis and treatment pathways,irrational use of antimicrobial drugs and high recurrence rate.How to optimize the hierarchical diagnosis and treatment pathway of urinary tract infection,standardize the use of antimicrobial drugs,and reduce the recurrence rate have always been the focus of clinical attention.There is significant heterogeneity in the existing diagnostic criteria for urinary tract infection,which seriously affects the comparability and evidence integration of clinical and research studies.In order to solve the above problems,a consensus on global multidisciplinary diagnostic criteria for urinary tract infection has been formed by international multidisciplinary experts after three rounds of Delphi method.Breaking through the traditional classification framework,the consensus innovatively established a four-dimensional quantitative scoring system including local symptoms and signs,systemic inflammatory response,quantitative analysis of pyuria and urine culture results,and established a hierarchical standard for stepwise urinary tract diagnosis according to the scoring threshold.Based on the key citations related to the consensus,this paper interprets in detail the basis for the selection of core indicators and the establishment of thresholds for the diagnosis of urinary tract infection in the consensus,and focuses on the key issues and implementation paths of the consensus in localization practice.This consensus provides a unified standard for standardizing the clinical diagnosis and treatment of urinary tract infection,improving the homogeneity of clinical research through standardized diagnostic processes,and promoting the standardization of UTI drug research and development and the rational use of antibiotics and precision.

Different animals in Xinjiang carry Escherichia coli O157:H7(E.coli O157:H7),but the connection between these strains is not clear.This study aims to understand the evolutionary sub-group of E.coli O157:H7,the distribution of the dominant genetic lineage,the biofilm formation ability,the carriage of mobile genetic elements and their drug resistance profile.E.coli O157:H7 was identified by PCR.Multilocus sequence typing(MLST)protocol was used for E.coli O157 to detect ST type,plasmid replicon and integron genes.Biofilm formation ability was determined by crystal violet microplate,and Kirby-Bauer was used to detect drug resistance.The results showed that 46.7％(7/15)of E.coli O157:H7 belongs to Group A,53.3％(8/15)of E.coli O157:H7 be-longs to Group E.Sheep source were mainly prevalent in Group A(4/6).Cattle sources are mainly Group E(6/7).A total of six ST types were detected:ST11(8/15),ST-206(1/15),ST-6126(3/15),ST-1640(1/15),ST-178(1/15),ST-4550(1/15).Two strains had a moderate biofilm-form-ing capacity,two strains had a weak biofilm-forming capacity,10 strains have no biofilm-forming capacity.All were multidrug-resistant strains,with complete resistance to lincomycin,oxacillin,clindamycin,vancomycin,midemycin and cefthiophene,and 88％-94％resistance to poly-myxin B,ampicillin,penicillin G and erythromycin,they are highly drug resistant.The five resist-ance genes detected were acrA(66.66％,10/15),tolC(73.33％,11/15),qurS(13.33％,2/15),floR and qurA(6.67％,1/15).Four plasm id replicons were detected,they were IncP(66.66％,10/15),IncFrepB(86.67％,13/15),IncFIA(6.67％,1/15),IncFIB(66.66％,10/15).Two class Ⅰ integrons were detected and they were ISCR1(33.33％,5/15),ISECP1(20％,3/15).The re-sults showed that E.coli O157:H7 in Xinjiang was predominantly prevalent in Group A and Group E.Sheep sources were predominantly prevalent in Group A,and cattle sources were predominantly prevalent in Group E.The ST types were widely distributed,with ST11 types being the predomi-nant type,the biofilm-forming ability was weak,and the resistance was strong,all of them were multi-drug-resistant strains,and the resistance genes were mainly externally excreted from the pumps,and the resistance genes had more spreading elements.

Objective This study aims to investigate the association between remnant cholesterol(RC)and the risk of metabolic-associated fatty liver disease(MAFLD)under the optimal triglyceride(TG)levels recom-mended by different guidelines.Methods The data were derived from the annual physical examinations of elderly people aged 65 and above in a community in 2023.Regression analysis was used to evaluate the association between RC and MAFLD risk.According to the TG normal level(<1.7 mmol/L)recommended by the Chinese Lipid Management Consensus and the TG ideal target(<1.2 mmol/L)proposed by the European Atherosclerosis Society,the individuals were divided into subgroups with different TG levels to explore the association between RC and MAFLD risk in each subgroup.Results A total of 2,800 elderly individuals aged 65 and above were included in this study.The proportion of the individuals meeting the diagnostic criteria for MAFLD was 20.85%,and RC was identified as an independent risk factor for MAFLD(P<0.001).In the elderly individuals with TG<1.7 mmol/L,RC level was not significantly associated with MAFLD risk(P=0.888).In contrast,in the elderly individuals with TG≥1.7 mmol/L,RC level was significantly and positively correlated with MAFLD risk(P<0.001).Interaction tests revealed no significant interaction between the stratification factor and the effect size of RC(P=0.115).In the elderly individuals with TG<1.2 mmol/L,RC level was not associated with MAFLD risk(P=0.505),while in the elderly individuals with TG≥1.2 mmol/L,RC level was significantly associated with MAFLD risk(P<0.001).Interaction tests showed a significant interaction between the stratification factor and the effect size of RC(P=0.011).Conclusion RC is an independent risk factor for MAFLD in older individuals.To reduce the risk of MAFLD related to RC in the elderly,a triglyceride level of<1.2 mmol/L can serve as a reference for identifying early-stage risk.

BACKGROUND:Neurodegenerative diseases are closely related to the imbalance of mitochondrial autophagy regulation.Previous studies by the research group have shown that lycium barbarum polysaccharide has neuroprotective effects,but whether it can improve the damage of SH-SY5Y cells induced byβ-amyloid protein 1-42 by regulating mitochondrial autophagy is still unclear.OBJECTIVE:To explore the protective effect and mechanism of Lycium barbarum polysaccharide on SH-SY5Y cells induced by β-amyloid protein 1-42.METHODS:An Alzheimer's disease cell model was established by inducing SH-SY5Y cells with β-amyloid protein 1-42,and then intervening with Lycium barbarum polysaccharide.SH-SY5Y cells were divided into three groups:control group,β-amyloid protein 1-42 group(20 μmol/L β-amyloid protein 1-42 for 24 hours),and Lycium barbarum polysaccharide group(1 g/L Lycium barbarum polysaccharide was added 1 hour in advance to form a protective effect,and then 20 μmol/L β-amyloid protein 1-42 was added to intervene with Lycium barbarum polysaccharide for 24 hours).CCK8 assay was used to detect cell viability.Mitochondrial membrane potential was detected by JC-1.TUNEL staining was used to detect cell apoptosis.Immunofluorescence and western blot assay were used to detect the expression of synaptic,apoptosis,and mitophagy-related indicators.RESULTS AND CONCLUSION:(1)Compared with the control group,the cell viability of the β-amyloid protein 1-42 group decreased(P＜0.05);cell apoptosis rate increased(P＜0.05);mitochondrial membrane potential decreased(P＜0.05);the expressions of pro-apoptotic proteins Bax and Caspase3 increased(P＜0.05);the expression of anti-apoptotic protein Bcl-2 decreased(P＜0.05);the expression levels of synaptic-related proteins Syn and PSD-95 decreased(P＜0.05);the expression levels of mitochondrial autophagy-related proteins Pink1,LC3A/B,Parkin,and Beclin-1 decreased(P＜0.05);and the expression of P62 increased(P＜0.05).(2)Compared with the β-amyloid protein 1-42 group,the cell viability in the Lycium barbarum polysaccharide group was increased(P＜0.05);the apoptosis rate was decreased(P＜0.05);the mitochondrial membrane potential was increased(P＜0.05);the expression levels of Bax and Caspase3 were decreased(P＜0.05);the expression of Bcl-2 was increased(P＜0.05);the expressions of Syn and PSD-95 were increased(P＜0.05);the expression levels of Pink1,LC3A/B,Parkin,and Beclin-1 were increased(P＜0.05),and the expression of P62 was decreased(P＜0.05).These findings indicate that Lycium barbarum polysaccharide may inhibit β-amyloid protein 1-42-induced damage to SH-SY5Y cells by regulating mitophagy,reduce cell apoptosis,and increase neuronal synaptic plasticity.

Objective:To investigate the neuroprotective effect of nicotinamide riboside(NR)on experimental autoimmune en-cephalomyelitis(EAE)mice.Methods:C57BL/6 female mice were induced by myelin oligodendrocyte glycoprotein(MOG35-55)to pro-duce EAE model and were randomly divided into EAE group and NR group.From day 3 to day 27 after immunization,each mouse in EAE group was given normal saline(200 μl/d)and each mouse in NR group was given NR(500 mg/kg,200 μl/d)by intragastric administration.Clinical score and body weight of mice in EAE group and NR group were recorded every day.On the 28th day after immunization,the spinal cord protein of mice in each group was extracted and the frozen sections of spinal cord of mice in each group were prepared.LFB staining was used to detect demyelination,immunofluorescence staining was used to detect the expression of MAP-2 and the number of positive cells of NeuN,BDNF,GDNF,NGF and NT-3,and Western blot was used to detect the expressions of BDNF,GDNF,NGF and NT-3 of spinal cord.Results:Compared with EAE group,NR significantly delayed the onset time of EAE mice(P<0.05),decreased clinical score(P<0.05),reduced weight loss,alleviated spinal cord demyelination(P<0.05),increased the expression of MAP-2(P<0.01)and the number of NeuN positive cells(P<0.01),and up-regulated the expressions of BDNF,GDNF,NGF and NT-3(P<0.05).Conclusion:NR shows a good neuroprotective effect on EAE mice.The mechanism may be related to NR significantly increasing the expression of spinal neurotrophic factors,improving the microenvironment of the central nervous sys-tem,nourishing nerves,promoting nerve repair and nerve growth,etc.